Dyspepsia

Moralising also has probably influenced attitudes to non-drug measures, implying that correction of pathological reflux is within the patient's control. This is untrue for most patients with significant disability from heartburn, as reflux results from intrinsic oesophageal motor defects,' the severity of which is only partly influenced by how the individual behaves. Not pressing therapy beyond an inadequate response to non-drug measures may sometimes be the result of a perception that the patient has made an inadequate effort to change things and that drug therapy is a "soft" option.

patients work this out without our help.
Moralising also has probably influenced attitudes to non-drug measures, implying that correction of pathological reflux is within the patient's control. This is untrue for most patients with significant disability from heartburn, as reflux results from intrinsic oesophageal motor defects,' the severity of which is only partly influenced by how the individual behaves. Not pressing therapy beyond an inadequate response to non-drug measures may sometimes be the result of a perception that the patient has made an inadequate effort to change things and that drug therapy is a "soft" option.
Inadequate management of heartburn also stems from inadequate knowledge about the efficacy of drug treatment. Antacids are sometimes convincingly effective in aborting heartburn episodes, but more often the response leaves much to be desired. In the only really rigorous clinical trial of regular antacid use for the treatment of reflux disease, the placebo antacid treated patients did better than those getting the real thing!9 If "p.r.n. antacid" does not control heartburn adequately within a few days, it should be abandoned.
By contrast, antireflux surgery and acid suppressant drugs can relieve heartburn totally in the complete spectrum of reflux disease patients. The efficacy of surgery has been known for a long time; acid suppression has achieved a very high level of efficacy only recently and this efficacy is only now becoming common knowledge. I:fficacy depends not only on the drug type, but also on how it is used. In Patients with endoscopically mild oesophagitis, heartburn responds well to standard dose H 2 receptor antagonists"'· or cisapride, a motility stimulant drug. More severe disease is relatively refractory, and the only effective drug therapy is higher-level acid suppression.' Double-dose famotidine and quadruple-dose ranitidine therapy are both moderately effective in troublesome reflux disease, but omeprazole at its standard dose of 20 mg/day has most effect on acid secretion and controls heartburn as well as oesophagitis in most cases.':" The new direction for management of heartburn requires recognition of the wide spectrum of efficacy from non-drug measures, antacids, cisapride, and standard-dose H 2 blocker, to high-level acid suppression, or anti reflux surgery.' Money is now the first major issue. Disabling heartburn should be Dyspepsia D yspepsia may represent the early symptom of a serious illness, such as peptic ulcer, gallstones or gastric . cancer. Often, however, there is no organic lesion.!" Dyspepsia can cause individual suffering, as well as an increased medical workload and significant financial cost. 3 The social and economic implications of dyspepsia have been studied in Scandinavia.' Extrapolating this data to Australia would give an annual cost of outpatient care and drugs of around 70 million dollars. If we take into account the cost of loss of earnings and sick leave benefits, the annual cost would exceed 400 million dollars.
Most people with dyspepsia do not seek medical advice, and the majority of those that do are treated in general practice.' controlled with the least expensive effective therapy, which ill mild cases may be lifestyle changes alone. When high levels of acid suppression are needed to control heartburn in younger patients, the expense and inconvenience of long-term therapy usually justify antireflux surgery, but the patient's preferences must be also considered. In older patients, high-level acid suppression is usually justified, as it breaks the "revolving door" pattern of frequent hospital attendances of patients with inadequately treated reflux disease, and greatly improves quality of life.
The possibility of gastric mucosal changes secondary to longterm, high-level acid suppression is the second major issue in modern therapy of severe reflux disease. This possibility has been raised by toxicological studies in rats subjected to lifelong massive dosage of omeprazole and ranitidine. " To date, there is no evidence that this is a practical concern in humans after up to five years of continuous omeprazole therapy.
Time, vigilance and marketplace competition will resolve the major issues of money and mucosae. At present these issues should be kept sight of, but despite them, effective relief of heartburn should now be a basic practice standard.
disorder. Despite its prevalence, there remains a lack of consensus in defining dyspepsia, its causes and its management. However it is defined, the term dyspepsia is embedded in our culture. In the broader sense, dyspepsia includes upper abdominal or retrosternal pain, discomfort, heartburn, nausea, vomiting or other symptoms referable to the proximal part of the alimentary tract. 9 Dyspepsia is ubiquitous throughout the community and frequently both patient and doctor are concerned that persistent symptoms indicate serious disease. The doctor treating a patient with dyspepsia is faced with two major questions.
Firstly, are there key symptoms present, which need immediate investigation?Certain symptoms (cardinal symptoms) indicate a high possibility of a serious organic disorder requiring treatment and should receive early investigation. Such symptoms include dysphagia, gastrointestinal bleeding, dyspepsia associated with significant weight loss, anorexia or anaemia, pain which wakes the patient from sleep, dyspepsia in a patient taking aspirin or non-steroidal anti-inflammatory agents, and dyspepsia in a patient with a history of peptic ulcer or with pain which radiates to the back.
Secondly, can symptoms be categorised to allow a rational decision on investigation and management? The large number of dyspeptic patients who, on investigation, do not prove to have any recognisable organic disease has stimulated attempts to establish categories of dyspepsia. After consideration of various International Working Party reports.v"': we suggest the following three categories: ulcer-like dyspepsia, reflux-like dyspepsia and motility-like dyspepsia.
Patients with ulcer-like dyspepsia have symptoms highly suggestive of peptic ulcer. A common clinical dilemma is posed by the patient with the "peptic ulcer likely" symptom complex, and a normal appearance on upper gastrointestinal endoscopy. Under such circumstances the doctor should proceed as follows. 1. Review the history to determine if there are symptoms which suggest an alternative category of dyspepsia.
2. Explain the situation to the patient and suggest lifestyle changes regarding smoking, alcohol, diet and concurrent medication (such as aspirin or non-steroidal anti-inflammatory drugs).
3. For persistent or severe symptoms, give an H, receptor antagonist for four weeks.
4. If the symptoms are not controlled by such a trial, look for Helicobacter pylori. If it is found one could contemplate eradication.
Helicobacter pylori causes inflammation of the gastric mucosa.'" 13 It is commonly identified in normal subjects (25%-35%), as well as those with non-ulcer dyspepsia (50%-60%) and duodenal ulcer (90%-100%)."·14 The role of H. pylori in ulcer-like dyspepsia remains unclear. Several placebo controlled trials have suggested that symptomatic improvement occurs with eradication of H. pylori from the gastric mucosa."·" Eradication may thus be beneficial in a subset of patients with severe refractory dyspepsia.
5. If all efforts fail, reappraisal and further investigation will be necessary.
The large reflux-like dyspepsia group includes all patients with heartburn and/or chest pain, as well as reflux or regurgitation. Symptoms suggestive of reflux-like dyspepsia are due to acid reflux into the lower part of the oesophagus and require acid suppression or neutralisation before other pathogenic factors are considered. This aim is achieved by antacid therapy, or the use of H 2 receptor antagonists, together with lifestyle changes including weight loss, dietary measures, cessation of smoking and review of potentially damaging medication (such as nonsteroidal anti-inflammatory drugs, antibiotics, antidepressants and slow-releasepotassium). If symptoms are not well controlled or "alarm symptoms" are present, then upper gastrointestinal endoscopy with oesophageal biopsy is mandatory. Cardinal symptoms in reflux-like dyspepsia include dysphagia, pain on swallowing liquids or solids, weight loss and anaemia.
In some series, up to one-third of patients with heartburn do not show endoscopic evidence of reflux oesophagitis. 17 . 18 However, a significant proportion of these patients will respond to conventional measures to treat acid reflux disease. Where endoscopy appearances have been completely normal, a therapeutic trial of H2 receptor antagonists with general lifestyle advice seems reasonable. Despite therapy, some patients remain symptomatic.
Where reflux-like dyspepsia involves chest pain and H2 antagonists have not been successful, the situation becomes complicated. Ultrasound is needed to exclude biliary disease, while electrocardiography, stress testing and possibly ventricular function studies may be needed to exclude cardiac disease. A small group of patients with distressing chest pain will need extensive investigation, including oesophageal motility studies and, in some cases, coronary angiography. Minor abnormalities may be found in some of these patients, but it will be sometimes difficult to arrive at a precise diagnosis.
The third category is motility-like dyspepsia. Australian studies have shown fairly equal numbers of patients with motility-like dyspepsia and reflux-like dyspepsia." Both these categories are far more common than ulcer-like dyspepsia. Motility-like dyspepsia is characterised by symptoms which suggest an underlying motility disturbance of the upper gut. Motility-like dyspepsia can be defined as upper abdominal pain and discomfort (usually poorly localised), plus two or more of the following: nausea and vomiting, early satiety and/or anorexia, postprandial abdominal bloating and/or feeling of distension, excessive repetitive post-prandial belching. Kellow's paper" is a timely reminder that this common group of patients with dyspepsia can be identified by recognition of the typical symptom cluster. If there are no alarm symptoms or signs, immediate investigation may not be warranted. Depending on the duration and severity of symptoms, it seems reasonable to reassure the patient that the probability of serious disease is low and explain the mechanisms believed to underlie the symptoms. Such reassurance in itself may often produce improvement. If the symptoms are still present after four weeks, upper gastrointestinal endoscopy is indicated.
In motility-like dyspepsia, psychosocial aspects may be important and sometimes psychological approaches to management may be warranted. It is important to diagnose untreated anxiety or depression, as these may alter response to other forms of therapy. Dietary changes can relieve postprandial symptoms. A reduced fat diet may be beneficial, as fat alters gastric motor function more than other dietary factors. Smaller meals and eating more frequently may be helpful.
If symptoms persist despite these measures, drug therapy needs consideration. On the available evidence, so-called "prokinetic agents" would appear to be the most useful in motility-like dyspepsia. As a rule, cisapride should be the first choice of medi-cation. Using prokinetic agents does notmean there is no role for suppressing acid in motility-like dyspepsia. For example, delayed gastric emptying which prolongs thecontact of acid with the gastric mucosa may be relevant. There may therefore be groups of patients who will respond totherapy to suppress acid, such as the use of H 2 antagonists.
Although thesymptoms ofdyspepsia arecommon and usually trivial, they sometimes can be quite chronic, dominating the patient's life, disrupting family or social relationships and resulting inconsiderable absence from work. Dyspepsia related to meals mayrequire alteration of eating habits, with avoidance of alcohol and many foods previously enjoyed. One-third of patients taking non-steroidal anti-inflammatory drugs may experience dyspepsia, sothat thesymptoms associated with one disease can be replaced by others as a result of therapy." Patients with dyspepsia tend to have a low threshold forpain, oran unusual dependence on medical help; nevertheless, their pain is real. They may havea heightened perception of normal physiological function." Sometimes it is possible to relate symptoms to periods of stress or major life events. Psychiatric illnesses are more common in patients with unexplained abdominal pain than in those with an organic disorder, particularly depression, anxiety andalcoholism." Thedoctor must also consider potential misuse of the health care system, such as narcotic addiction or false medical disability status.
Many patients, especially those under 45 years of age, may be overinvestigated, in order to exclude evidence of serious disease. Patients should be given a clear explanation of the mechanisms underlying their symptoms and the reasons for investigation. It should be stressed that, although some tests are necessary, it will not be surprising if the results prove to be normal. Many patients with dyspepsia have an inordinate fear of heart disease or cancer, particularly those with family or friends who have suffered or died from these diseases, and investigation tends to exacerbate the patient's concern about disease.
This categorisation of dyspeptic patients is sure to undergo further refinement as studies such asthatof Kellow· unravel the complex electrophysiological and hormonal events thatcontrol motility and secretory activity. Furthermore, correlation between clinical events and electrophysiological disturbance should provide future insights into this challenging area.

Terry D Bolin
Gastrointestinal Unit Prince of Wales Hospital, Sydney

Melvyn G Korman
Gastroenterology Unit Monash Medical Centre, Melbourne